Respiratory Failure

Background
Respiratory failure is a syndrome in which the
respiratory system fails in one or both of its gas
exchange functions: oxygenation and carbon dioxide
elimination. In practice, it may be classified as either
hypoxemic or hypercapnic.
 Background
Hypoxemic Respiratory Failure (Type I)
The most common form and can be associated with all
acute diseases of the lung, ie pulmonary edema,
pneumonia, and pulmonary hemorrhage

Hyper capnic Respiratory Failure (Type II)

common in patients with hypercapnic respiratory failure
who are breathing room air. The pH depends on the
level of bicarbonate, which, in turn, is dependent on the
duration of hypercapnia. Common etiologies include
drug overdose, neuromuscular disease, chest wall
abnormalities, and severe airway disorders
 Background
Respiratory failure may be further classified as either
acute or chronic

The clinical markers of chronic hypoxemia, such as

polycythemia or cor pulmonale, suggest a long-standing
disorder.

Other tests: Arterial blood gases, Chest radiography,

Echocardiography, Pulmonary functions tests,
Electrocardiography
 Pathophysiology
Airways, alveoli, central nervous system (CNS),
peripheral nervous system, respiratory muscles, and
chest wall.

Hypoperfusion secondary to cardiogenic, hypovolemic,

or septic shock often present with respiratory failure
 Pathophysiology
Ventilatory capacity is the maximal spontaneous ventilation
that can be maintained without development of respiratory
muscle fatigue. Ventilatory demand is the spontaneous
minute ventilation that results in a stable PaCO2.
Normally, ventilatory capacity greatly exceeds ventilatory
demand. Respiratory failure may result from either a
reduction in ventilatory capacity or an increase in
ventilatory demand (or both). Ventilatory capacity can be
decreased by a disease process involving any of the
functional components of the respiratory system and its
controller. Ventilatory demand is augmented by an increase
in minute ventilation and/or an increase in the work of
breathing.
 Respiratory Physiology
The act of respiration engages the following
three processes:
Transfer of oxygen across the alveolus
Transport of oxygen to the tissues
Removal of carbon dioxide from blood into the alveolus
and then into the environment
 Respiratory Physiology
Gas exchange
Respiration primarily occurs at the alveolar capillary
units of the lungs, where exchange of oxygen and
carbon dioxide between alveolar gas and blood takes
place.
The quantity of oxygen combined with hemoglobin
depends on the level of blood PaO2. This relationship,
expressed as the oxygen hemoglobin dissociation curve,
is not linear but has a sigmoid-shaped curve with a steep
slope between a PaO2 of 10 and 50 mm Hg and a flat
portion above a PaO2 of 70 mm Hg.
 Respiratory Physiology
Gas exchange
The carbon dioxide is transported in 3 main forms: (1)
in simple solution, (2) as bicarbonate, and (3) combined
with protein of hemoglobin as a carbamino compound.
During ideal gas exchange, blood flow and ventilation
would perfectly match each other, resulting in no
alveolar-arterial oxygen tension (PO2) gradient.
High-V/Q units
Low-V/Q units
 Respiratory Physiology
Alveolar ventilation
The rate of carbon dioxide production by the tissues is
constant and equals the rate of carbon dioxide
elimination by the lung. This relation is expressed by
the following equation:

VA = K × VCO2/ PaCO2
 Respiratory Physiology
Alveolar ventilation
The efficiency of lungs at carrying out of respiration can
be further evaluated by measuring the alveolar-arterial
PO2 gradient. This difference is calculated by the
following equation:

PAO2 = FiO2 × (PB – PH2 O) – PACO2/R

o an increase in the alveolar-arterial PO2 gradient above

15-20 mm Hg indicates pulmonary disease as the cause
of hypoxemia.
Hypoxemic Respiratory Failure
Two mechanisms:
V/Q mismatch
Shunt

These 2 mechanisms lead to widening of the alveolar-

arterial PO2 gradient, which normally is less than 15
mm Hg.

They can be differentiated by assessing the response to

oxygen supplementation or calculating the shunt
fraction after inhalation of 100% oxygen.
Hypoxemic Respiratory Failure
V/Q mismatch
Low V/Q unitshypoxemia and hypercapnia
Low V/Q unitsdecrease in ventilation or
overperfusion
high-V/Q units waste ventilation but do not affect gas
exchange unless the abnormality is quite severe.
Give 100% oxygen!
Hypoxemia increases minute ventilation by
chemoreceptor stimulation, but the PaCO2 generally is
not affected
Hypoxemic Respiratory Failure
Shunt
Persistence of hypoxemia despite 100% oxygen
inhalation.
The deoxygenated blood (mixed venous blood) bypasses
the ventilated alveoli and mixes with oxygenated blood
that has flowed through the ventilated alveoli,
consequently leading to a reduction in arterial blood
content. The shunt is calculated by the following
equation:
QS/QT = (CCO2 – CaO2)/CCO2 – CvO2)
Hypoxemic Respiratory Failure
Shunt
A normal right-to-left shunt may occur from atrial septal
defect, ventricular septal defect, patent ductus
arteriosus, or arteriovenous malformation in the lung.
Cause primarily by pneumonia, atelectasis, and severe
pulmonary edema
Hypercapnia does not develop unless shunt is excessive
(>60%)
 Hypercapnic Respiratory
Failure
At a constant rate of carbon dioxide production,
PaCO2 is determined by the level of alveolar
ventilation according to the following equation

PaCO2 = VCO2 × K/VA

• As ventilation decreases below 4-6 L/min, PaCO2 rises

precipitously
 Hypercapnic Respiratory
Failure
Decrease alveolar ventilation, can result from:
reduction in overall (minute) ventilation
increase in the proportion of dead space ventilation

In pure hypercapnic respiratory failure, the hypoxemia

is easily corrected with oxygen therapy

Hypoventilation is characterized by hypercapnia and

hypoxemia
 Etiology
Common causes of type I (hypoxemic) respiratory failure include the
following:

COPD Pneumoconiosis

Pneumonia Granulomatous lung diseases

Pulmonary edema Cyanotic congenital heart disease

Pulmonary fibrosis Bronchiectasis

Acute respiratory distress syndrome

Asthma (ARDS)

Pneumothorax Fat embolism syndrome

Pulmonary embolism Kyphoscoliosis

Pulmonary arterial hypertension Obesity

 Etiology
Common causes of type II (hypercapnic) respiratory failure include the
following:
COPD Porphyria

Severe asthma Cervical cordotomy

Drug overdose Head and cervical cord injury

Poisonings Primary alveolar hypoventilation

Myasthenia gravis Obesity-hypoventilation syndrome

Polyneuropathy Pulmonary edema

Poliomyelitis ARDS

Primary muscle disorders

 History
Confirmation of the diagnosis is based on arterial
blood gas analysis
The cause of respiratory failure is often evident after a
careful history and physical examination
A study by Canet et al, examining acute respiratory
failure in kidney transplant recipients, determined that
200 of 6,819 kidney transplant recipients required
admission to the intensive care unit (ICU) for acute
respiratory failure, which was associated with high
mortality and graft loss rates.
 Physical Examination
The signs and symptoms of acute respiratory failure
reflect the underlying disease process and the
associated hypoxemia or hypercapnia

Asterixis, tachycardia, arrhythmias, cyanosis

(concentration of deoxygenated hemoglobin in the
capillaries or tissues is at least 5 g/dL), dyspnea,
confusion and somnolence, myoclonus and seizures

Pulmonary hypertension frequently is present in

chronic respiratory failure
 Physical Examination
Criteria for the diagnosis of ARDS include the following:
Clinical presentation - Tachypnea and dyspnea; crackles upon
auscultation
Clinical setting - Direct insult (aspiration) or systemic process
causing lung injury (sepsis)
Radiologic appearance - 3-quadrant or 4-quadrant alveolar
flooding
Lung mechanics - Diminished compliance (<40 mL/cm water)
Gas exchange - Severe hypoxia refractory to oxygen therapy
(ratio of arterial oxygen tension to fractional concentration of
oxygen in inspired gas [PaO 2/FiO 2] <200)
Normal pulmonary vascular properties - Pulmonary capillary
wedge pressure lower than 18 mm Hg
 Approach Consideration
Arterial blood gases

Chest radiography

Echocardiography

Pulmonary functions test

Electrocardiography
 Laboratory Studies
Arterial blood gas analysis

Complete blood cell count

Creatine kinase and troponin I

TSH
Radiography
Radiography
Radiography
Radiography
 Echocardiography
The findings of left ventricular dilatation, regional or
global wall motion abnormalities, or severe mitral
regurgitation support the diagnosis of cardiogenic
pulmonary edema

Echocardiography provides an estimate of right

ventricular function and pulmonary artery pressure in
patients with chronic hypercapnic respiratory failure.
Pulmonary Function Tests
Patients with acute respiratory failure generally are
unable to perform PFTs; however, these tests are useful
in the evaluation of chronic respiratory failure.

FEV1, FVC, FEV1 -to-FVC ratio

Respiratory failure is uncommon in obstructive

diseases when FEV1 is greater than 1 L and in
restrictive diseases when FVC is greater than 1 L.
 Medication
Diuretics : Furosemid
Nitrates
Opioid analgesics : Morphine sulfate
Inotropic agents : Dopamine, norepinephrine, dobutamine
Beta2 Agonists: Terbutaline, albuterol
Xanthine derivatives: Theophylline
Anticholinergics: Ipratoprium bromide
Corticosteroids: Methylprednisolone
THANKS
 References
Kaynar AM. Respiratory failure. Available from:
https://emedicine.medscape.com/article/167981-
overview [Accessed 22th december 2017]